An Infant with Toxoplasmosis
Retinochoroiditis: A Case Report from
James E. Eullaran1, Ma. Delta S. Aguilar1,2 and Genelynne J. Beley1,2*
1Southern Philippines Medical Center, Department of Pediatrics, Davao City, Philippines
2Davao Medical School Foundation, Inc, College of Medicine, Department of Pediatrics, Davao City, Philippines
Submission: May 09, 2023; Published: May 17, 2023
*Corresponding author: Genelynne J. Beley, Southern Philippines Medical Center, Department of Pediatrics, Davao City, Philippines,Email:firstname.lastname@example.org
How to cite this article:James E. E, Ma. Delta S. A, Genelynne J. B. An Infant with Toxoplasmosis Retinochoroiditis: A Case Report from the Philippines. Acad Acad J Ped Neonatol 2023; 12(4): 555899. 10.19080/AJPN.2023.12.555899
Toxoplasmosis is a major and preventable cause of severe visual handicap and blindness among young people. More specifically, Toxoplasmosis retinochoroiditis (TRC) caused by Toxoplasma gondii is a rare but serious manifestation of toxoplasma infection. There are only two probable means of acquiring the disease, through the congenital route and acquired. In the Philippines, there are only a few reported cases and studies about TRC in the human population. With this, there is also a paucity of available therapy for this condition. Diagnostic tools for TRC are not readily available in most areas in the Philippines. This report is a classic Toxoplasma infection in a 9-month-old patient presenting with subtle eye symptoms. The use of serologic markers supported the initial impression.
In pediatrics, strabismus is a common condition. Males and females may have strabismus, and may have genetic influences . An infant’s ability to control their eye movement should be fully developed by the age of four months. A child with strabismus, will have an eye that is out of alignment, which causes a discrepancy in the visual impulses reaching the brain. Loss of depth perception will occur because the brain will ignore the image of the misaligned eye and concentrate on the image of the straight eye . It is crucial to detect strabismus in children since it can lead to visual and emotional problems. Children who are at high risk for eye problems should be referred to an ophthalmologist for a screening exam. It is crucial to identify children who have obvious strabismus since, if untreated, they have a higher risk of amblyopia. The development of strabismus is multifactorial with both genetic and environmental influences. There are congenital and acquired forms of strabismus, and it’s critical to distinguish between the two because some acquired forms of strabismus pose a risk to one’s life or vision. Birth history, genetics, neuromuscular disorders, malignancies, structural eye problems, trauma, infections, systemic ailments with eye-threatening symptoms, and iatrogenic causes are the prevalent risk factors associated with strabismus among pediatric age groups .
This is a case of a 10-months old, female infant from Surigao, Philippines, who was brought for evaluation due to occasional wandering of the left eye or squinting. The patient has been apparently well until at four months of life, when occasional wandering of the left eye was noted. No consultation was done for this. However, the wandering of the eye persisted until the patient was 9 months old. There was no history of trauma, leukocoria, eye redness, fever, or seizures. They sought consult at an eye center in their locality. Two ophthalmologists were able to examine her. A “white matter” on the patient’s left eye was seen, hence B scan was requested.
B scan done showed a macular scar versus beginning ocular mass. Follow-up consults was advised.
Two months prior to consultation, a Ret Cam was done at
Southern Philippines Medical Center (SPMC) where a characteristic
calcification was noted (Figure 1). The Ophthalmology service
strongly considered a parasitic cause of the eye condition linked
to a certain zoonotic parasite. Further history revealed presence
of adopted eight cats, some are stray with six dogs, of which two
are Belgian Malinois, and six are native-origin dogs. With this, a
serum IgM and IgG titer were done with subsequent referral to the
pediatric infectious service.
Prenatal and birth history were unremarkable with normal
Expanded Newborn Screening and Hearing Tests. Patient was
previously diagnosed with COVID-19 mild along with all of
the seven family members. The family underwent quarantine
protocols. Feeding and immunization status were according to the
recommendation of the Philippine Pediatric Society adequate for
her age. Developmental milestones are at par with age and family
history has hypertension on both maternal and paternal side.
Pertinent social history is the family’s love for pets. They have
eight cats which roam inside the house and around the village.
Moreover, the patient’s grandfather regularly feeds their own
cats as well as stray cats. They also have six dogs. All the dogs are
vaccinated with anti-rabies and dewormed. However, the pet cats
On physical examination, patient was examined at the outpatient
department with stable vital signs: blood pressure of
90/60 mm Hg, heart rate of 102 beats per minutes, respiratory
rate of 22 cycles per minute, temperature of 36.8 degrees Celsius.
Patient’s weight is 8 kilograms and length of 71 centimeters
revealing a normal anthropometric measurement.
Pertinent findings of the eyes revealed presence of white
sclera and pinkish palpebral conjunctiva. Pupils are 4mm in size
constricting to 2mm, equally round and reactive to light and
accommodations. There is a noticeable inward deviation of the
left eye (Figure 2). Detailed ophthalmologic examination by the
Ophthalmology Department revealed presence of whitish flat
lesion with smooth surface and irregular borders at the area of
the macula on the left eye (Table 1). The rest of the systems are
Patient’s work-ups were done as ambulatory. Toxoplasmosis
titer for IgG revealed positive confirming the infection of
Toxoplasmosis retinochoroiditis (Table 2).
Patient was subsequently managed as a case of Toxoplasmosis
retinochoroiditis and was referred to Pediatric Infectious Disease
Service for co-management. Cranial CT scan was requested to
further rule out extra-organ seeding of the disease. Treatment
plans include starting her on Pyrimethamine 2mkD loading
dose and 1mkD maintenance dose for 2 months, Trimethoprim-
Sulfamethoxazole (TMP-SMX) 12mkD twice a day for 2 months, folic Acid 1mkD once a day for 2 months, and Complete Blood Count monitoring every 2 weeks once the patient is on treatment.
The unavailability of Pyrimethamine in the Philippines is a
challenge, hence intravenous TMP-SMX administration in lieu of
Pyrimethamine is the next option.
Toxoplasmosis is an infection of the retina caused by the
protozoan Toxoplasma gondii that affects both immune-suppressed
individuals and healthy individuals globally. It is lethal for those
with weakened immune systems. Children with immunologically
sound immune systems may have no symptoms from an acute
acquired infection, which can also result in lymphadenopathy and
may affect other organs . T. gondii, a member of the phylum
Apicomplexa, has a polar apical complex that mediates attachment
to the host cell membrane. Once acquired, the latent encysted
organisms will persist in the host throughout life.
Bone marrow transplant recipients may develop systemic
illness as a result of immune-compromised patients regularly
experiencing CNS-related signs and symptoms. Congenitally
acquired toxoplasmosis can cause chorioretinitis and
abnormalities in the CNS during pregnancy or later in life if it is
left untreated .
The parasite is spread by eating uncooked meat that contains T.
gondii cysts or feces-derived oocyst-containing water.7 In countries
with a range of cultural, socioeconomic, and ethnic origins, the
illness has been seen to spread through both water and food. It
is possible for the parasite to spread vertically, most frequently in
situations of primary sickness in pregnant women. Despite being
rare, transplanted organs have the potential to spread the illness.
The most likely cause of the sickness in this case is swallowing
a medium containing oocyst from their pet cats’ litters . The
patient’s family owns 10 cats at home and this is likely the source
of the patient’s infection.
T. gondii is a single-cell, obligate, intracellular protozoan
parasite. The cats are the definitive host but humans and several
of mammals, birds, and reptiles, may also serve as intermediate
hosts. T. gondii has three forms: a. the oocyst (soil form), b. the
tachyzoite (active infectious form), and c. the tissue cyst (latent
form) . This coccidian protozoan multiplies in living cells. The
tachyzoites are 2-4 x 4-7 um and are oval and crescent-shaped.
Skeletal muscles, central nervous system and cardiac muscles are
the areas where tissue cysts, 10-100 um in diameter are found
. These cysts will remain in those tissues . The T. gondii life
cycle is divided into two parts: an asexual phase, which takes
place in nucleated cells; and a sexual phase through schizogonic
and gametogenic cycles within the distal ileal epithelium of
the cat intestine. Fertilized gametes are created during sexual
reproduction in the feline’s small intestine and are then ejected as
two-sporocyst oocysts, which may survive in the environment for
up to 18 months with the right humidity and temperature. Each
sporocyst matures into four sporozoites. For about two weeks,
the cat excretes 105 to 107 oocysts daily. Oocysts turn infectious
after sporulating 1–5 days after release. When swallowed oocysts
or tissue cysts rupture, they enter the intestinal lining cells and
release sporozoites or bradyzoites, which later transform into
tachyzoites, the parasite’s form that reproduces quickly. The host’s
leukocytes may contain these tachyzoites or they may be freely
circulating through the circulation. Once the intestinal mucosa
has been breached, tachyzoites move through the patient’s blood
and lymphatic system to distant organs like the brain, liver, spleen,
lymph nodes, heart, skeletal muscles, placenta, and eyes. Another
hypothesis is that the parasite enters the brain and eye after being
directed by dendritic cells and macrophages over the blood-brain
Worldwide, over 6 billion people have been infected with T.
gondii. Seroprevalence, measured by IgG against T. gondii, varies
in different countries, 6.7% in Korea , 12.3% in China ,
23.9% in Nigeria , 46% in Tanzania  and 47% in France
(rural area), and it can be as high as 98% in some regions .
Reports with low seroprevalence are from Southeast Asia, North
America and Northern Europe with 10-30%. Prevalence between
30 and 50% have been reported for Central and Southern Europe,
whereas high seroprevalences are observed in Latin America and
in tropical African countries. The different seropositivity rates
largely depends on the prevalence of T. gondii cysts and oocysts in
the environment . This infection is more common in countries
with humid temperatures such as Asia, the Caribbean region and
in Central America .
It commonly occurs in healthy children or young adults in 75%
of cases, often during puberty. Toxoplasmosis gondii has an affinity
for the nervous tissue, particularly involving the retinal ganglion
cells in the eye .
One study was conducted in Cebu. out of 924 participants,
244 (26.4%) were found to be seropositive from 21 different
municipalities and cities in Cebu. Seropositivity was found to
be greater among women (27%) than men (25.5%) . For
toxoplasmosis retinochoroiditis alone, the seropositivity is
between 20% to 70% in the United States while the incidence of
Toxoplasma retinochoroiditis is 0.6% . Several studies from
around the world have shown that ocular toxoplasmosis is the
most common form of posterior uveitis. In certain groups, ocular
toxoplasmosis is the primary cause of uveitis. Ocular toxoplasmosis
is likely underdiagnosed in many countries with endemic T. gondii
infection . It has long been thought that postnatal infections
seldom cause symptoms and that prenatal infections are the main
cause of ocular toxoplasmosis. This paradigm was challenged
by research from Brazil that revealed postnatal infection and
toxoplasmosis ocular symptoms were more common than
congenital infection. This finding was confirmed by other groups
and likely applies to most populations exposed to T. gondii .
When ocular toxoplasmosis manifests with the traditional
ophthalmological symptoms, a clinical examination is employed
to determine the diagnosis rather than a laboratory test to
confirm parasite infection. A history of systemic exposure to the parasite is indicated by toxoplasmosis seropositivity, however this information is inadequate to make the diagnosis. Although retinal
lesions in the retina’s periphery frequently result to secondary
severe vitreous inflammation and vision loss, macular lesions may
also cause secondary visual impairment. Optic nerve involvement
can cause substantial visual field anomalies and color vision
loss, though less frequently. Active lesions’ primary symptom,
which is vision blurring, is connected to symptomatic vitreous
inflammation. The size and location of retinochoroidal scars are
negatively connected with scotomas during the parasite’s latent
A nidus of fluffy white, focal necrotizing retinitis or
retinochoroiditis next to a chorioretinal scar with a range of
pigmentations is the classic visual presentation of toxoplasmosis.
The traditional “headlight in the fog” indication is frequently
caused by a strong vitritis that hides the active lesion. The
posterior segment involvement may be hidden by the anterior
uveitis, which can range in intensity from a mild response to
a severe inflammation. Other common clinical signs of ocular
toxoplasmosis include satellite lesion, retinochoroidal scar, focal
or widespread vasculitis, and inflammatory ocular hypertension
syndrome . Multifocal retinochoroiditis, low-grade or absent
vitreal infiltration, an active lesion larger than two disk diameters
without an accompanying retinochoroidal scar, absence of a
retinochoroidal scar, bilaterality, involvement of the optic disk,
choroiditis without retinitis, hemorrhagic vasculitis, serous
retinal detachment, and retinal neovascularization are examples
of abnormal findings . The patient in this case presented
with a macular scar versus beginning intraocular mass with
calcifications highly characteristic of toxoplasmosis.
In cases of congenital toxoplasmosis, the mother may have been
asymptomatic or have had mild mononucleosis-type symptoms. In
contrast, the newborn may exhibit with prematurity, intrauterine
growth restriction, jaundice, hepatosplenomegaly, myocarditis,
pneumonitis, various rashes and neurologic findings that
include chorioretinitis, hydrocephalus, intracranial calcifications,
microcephaly, and seizures. Some of the neurological symptoms
may only become apparent months to years later. The classic triad
of neurological findings consists of chorioretinitis, hydrocephalus,
and intracranial calcifications .
Toxoplasmosis Retinochoroiditis should be differentiated
from other conditions such as retinoblastoma which presents
commonly with leukocoria and with a biopsy finding of Flexner-
Wintersteiner rosettes4 characteristic of the malignancy. Intake
or exposure to lead and other toxins should be ascertained. It
can cause neurologic manifestations and could eventually lead
to ocular symptoms such as strabismus . Guillain-Barre,
Myasthenia Gravis, and Multiple Sclerosis are neuromuscular
autoimmune disorders which manifest also with strabismus .
However, extraocular manifestations are more prominent in these
cases. Presence of specific antibodies supports its diagnosis.
Basing in the clinical presentation, the diagnosis of ocular
toxoplasmosis is frequently obvious. When a funduscopic
examination cannot definitively determine the clinical diagnosis,
serological testing, such as serum anti-Toxoplasma titers of IgM
and IgG, may be required to support the diagnosis. T. gondii
antibody titers in ocular fluids or polymerase chain reaction (PCR)
of aqueous and vitreous samples are other newer tools with high
sensitivity and specificity to confirm the diagnosis [3,14].
The majority of diagnostic laboratories can only use
commercial ELISA (enzyme-linked immunosorbent assay) or
immunofluorescent antibody kits to measure IgG and IgM antibody
levels. Because ELISA allows for automation and the simultaneous
testing of numerous samples, it is preferable to immunofluorescent
antibody testing because the results are objective. The Sabin-
Feldman dye test, the classic gold standard serology test, uses live
T. gondii tachyzoites to detect IgG antibodies.
Serum IgM and IgG antibodies to T. gondii develop within 1-2
weeks after infection. IgG serology may be the first test performed
on patients suspected of having acute toxoplasmosis; if IgG
results are positive, IgM antibody levels may also be assessed.
In an immunocompetent patient, nonreactive IgG rules out the
toxoplasmosis diagnosis. IgM levels increase during the first week
and decrease after 6 to 9 months. A recent infection should not
be inferred just from elevated antibody levels, and an inactive
illness should not be inferred from low blood IgG levels. Levels of
serological tests should be redone in 15–21 days if the lab results
are clear .
A latent infection with a history of initial exposure may
exist in asymptomatic individuals with IgG reactivity alone.
This serological pattern determines the likelihood of illness
recurrence in immunosuppressed individuals, including those
with HIV infection and transplant recipients . In patients with
reactivation disease, IgM and IgG response may not be seen.
Additional tests to rule out Toxoplasma infection should be
carried out in immunocompromised patients with seronegativity
but strong clinical evidence. These consist of T. gondii PCR of the
vitreous and aqueous humor or IgG antibody testing .
The patient in this case has a positive Toxoplasma IgG titer and
normal borderline high Toxoplasma IgM titer. Recently, serologic
tests served as the primary means of diagnosis. We can conclude
that this patient has a toxoplasma infection since IgG specific
antibodies achieve a peak concentration 3 to 5 months after
infection and remain positive indefinitely. This coincides with the
patient’s symptom presentation which started 5 months prior to
consultation. With the negative IgM serologic titer, this is not a
recent, chronic latent infection, or a false-positive reaction.
The clinical features of a group of patients with ocular
toxoplasmosis were compared in research by Rodanes et al. based
on the patients’ IgM status. It should be highlighted that the group that tested positive for IgM at presentation had bigger lesions, a higher incidence of macular involvement, and higher levels of
intraocular inflammation. In contrast to this study, the patient
had a normal or borderline high IgM titer and no additional
inflammatory signs .
Assessment of the risk of transplacental transfer also
uses serology. In nations where toxoplasmosis is an endemic
disease, IgG serology is regularly conducted on women who
are contemplating pregnancy. Immunocompetent women who
have elevated IgG levels before to conception have a reduced
likelihood of transplacental transfer. It is suggested that those
with undetectable IgG levels stay away from eating raw meat or
cat excrement. Acute infection in the last six months is excluded by
negative IgM serology; if it is positive, it may linger for up to two
years following T. gondii exposure .
Biopsy is not frequently done but in atypical cases, it helps in
the diagnosis. A necrotizing retinitis occurs with vasculitis and
destruction of the retina is commonly appreciated .
Treatment and Management
Except in cases where it is proven that the infection occurred
during pregnancy, there is ocular involvement, or the symptoms
are severe or persistent, the majority of cases of acquired acute
toxoplasmosis in immunocompetent hosts do not require
specific therapy. Moreover, treatment of acute toxoplasmosis in
immunocompromised patients is always recommended. Given
this, treating the patient’s condition is only prudent. For children
with active toxoplasmosis chorioretinitis, treatment should be
initiated right away since it is a medical emergency. When the
disease is still in its active stage, they are administered along with
pyrimethamine, sulfadiazine, and leucovorin for about a week
after the lesion has assumed a quiescent appearance, such as sharp
borders, pigmentation at the lesion’s margins, and resolution of
associated inflammatory cells in the vitreous, which typically takes
place in 2-4 weeks when treatment is initiated promptly. The edges
of the retinal lesions get sharper after 7–10 days, and visual acuity
becomes normal. When the macula, optic nerve head, or retina
are affected, corticosteroids are given together with antibacterial
therapies . This should not be given alone and must be started
after the initiation of pyrimethamine and sulfadiazine for 2 days.
As for this patient, pyrimethamine, TMP-SMX, and Folic acid are
proposed to be started. With difficulty in the procurement of
pyrimethamine, intravenous route of administration of TMP-SMX
in lieu of pyrimethamine is an alternative. TMP-SMX in intravenous
form has been reported to be equivalent to pyrimethamine/
Performing a vitrectomy and removing the lens to improve
vision is extremely uncommon. In addition to oral anti-toxoplasma
medications, intravitreal injection of an antibody to vascular
endothelial growth factor has been effective for those with active
choroidal neovascular membranes .
Within a few years of the initial infection, the likelihood of
toxoplasmosis retinochoroiditis reactivation from pre-existing
chorioretinal scars increases, with a relatively rapid decline in
the incidence of reactivations over time. According to one study,
TRC recurrence occurs at a rate of 50% over three years and 80%
over five years, with an average lifetime recurrence of 2.7 episodes
[3,14]. Other anticipated outcomes include vision impairment of
less than 20/40. Additionally, there was a significant decline in
verbal and geometric design aspects of the intelligence quotient
The majority of cases of toxoplasmosis are avoidable. One of
its consequences, toxoplasmosis retinochoroiditis, is extremely
uncommon and challenging to treat. Therefore, it is necessary
to follow hygienic procedures at first. Litter boxes and areas
frequented by cats, particularly sand or soil in gardens or
playgrounds, present a serious risk and have to be avoided. It is
advised to regularly clean fruits and vegetables and to wash your
hands after coming into touch with soil or cat litter boxes. Food
should be handled properly since toxoplasma cysts are destroyed
at 60 degrees C for 15 minutes or by -20 degrees C for at least
24 hours. Oocyst-tainted water is now a widely recognized way to
contract acquired toxoplasmosis in places with insufficient water
treatment. However, an interprofessional team composed of an
ophthalmologist, neurologist, and infectious disease specialist is
best suited to manage toxoplasmosis retinochoroiditis if it has
already manifested. Immunosuppressed patients typically require
long-term care and monitoring. Preventive measures including
staying away from cat-friendly environments, must be explained
to patients and primary caregivers. Patients with TRC have a
Faap M. D. K. W., M.D., B. E., Faap, L. R. M., & Faap, M. M. S. H. (2021) Red Book 2021: Report of the Committee on Infectious Diseases (Thirty-second ed.). American Academy of Pediatrics.
Roizen N, Kasza K, Karrison T, Mets M, Noble AG, et al. (2006) Impact of visual impairment on measures of cognitive function for children with congenital toxoplasmosis: implications for compensatory intervention strategies. Pediatrics 118(2): e379-e390.